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Supraventricular tachycardia
Caroline Medi, Jonathan M Kalman and Saul B Freedman
S upraventricular tachycardia (SVT) refers to a range of condi-
tions in which atrial tissue or the atrioventricular node is
essential for sustaining an arrhythmia. This review focuses on
the three most common types of SVT — atrioventricular nodal re-
entrant tachycardia (AVNRT), atrioventricular re-entrant tachycar-
dia (AVRT) and atrial tachycardia (AT); it also describes inappro-
priate sinus tachycardia and postural orthostatic tachycardia
syndrome, forms of sinus tachycardia (Box 1). Other types of SVT
include atrial fibrillation and atrial flutter, which were the focus of
1
a recent
Theclinical
Medicalupdate in of
Journal theAustralia
Journal.ISSN: 0025-
The729X
incidence of SVT is about 35 cases per 100 000 population
2 March 2009 190 5 255-260
per year,
©The with a prevalence
Medical Journalofof2.25 cases per
Australia 1000 population.2
2009
SVT usually manifests
www.mja.com.au as recurrent paroxysms of tachycardia. It is
Review
generally well tolerated but can produce uncomfortable symptoms
that lead to acute presentation.
Clinical features
Younger patients with SVT usually have structurally normal hearts,
and are more than twice as likely to be female as male.3 Most females
with SVT present during their childbearing years (15–50 years),4
and this has been linked to the effect of progesterone on the
myocardium.5 Women with SVT are more likely to have AVNRT
than men,4 whereas there is a male predominance in AVRT.6
For the three most common types of SVT, peak incidence of
presentation for ablation occurs in the middle decades of life: at 36
years for AVRT, 48 years for AVNRT, and 50 years for AT.7 The
proportion of SVT caused by AVRT declines progressively with
age, from 60% during the first decade of life to 9% after age
70. Correspondingly, there are steady increases in the propor-
tions of AVNRT (from 33% to 68%) and AT (from 7% to 23%).
In one study, AVNRT replaced AVRT as the dominant paroxys-
mal SVT mechanism at age 40 in males and at age 10 in
females. 7 A significant proportion of patients have symptoms for a
prolonged period (> 1 year) before the diagnosis of SVT is made,
and occasionally episodes are misdiagnosed as anxiety or panic
disorders.8 These misdiagnoses occur more frequently in women.
Symptoms
Palpitations and pounding in the neck or head are the most
common symptoms of SVT, and may be accompanied by chest
discomfort (chest pain is unusual), dyspnoea, anxiety, lightheaded-
ness or, uncommonly, syncope. Syncope may occur at onset,
before autonomic reflexes respond to blood pressure fall, particu-
larly when heart rate is very rapid and occasionally during very
prolonged episodes. It may also occur in response to rapidly
conducted atrial fibrillation via an accessory pathway, or when SVT
occurs in the presence of significant structural heart disease.
The severity of symptoms is highly variable and depends on
features including heart rate, duration of tachycardia, underlying
heart disease, and individual patient perception. Incessant SVT can
result in tachycardia-mediated cardiomyopathy.9 This left ventricu-
lar dysfunction is usually completely reversible on control or cure
of the arrhythmia.10 SVT occasionally results in myocardial isch-
aemia, or precipitates cardiac failure in patients with pre-existing
MJA • Volume 190 Number 5 • 2 March 2009
ABSTRACT
• Supraventricular tachycardia (SVT) is a common cardiac rhythm
disturbance; it usually presents with recurrent episodes of
tachycardia, which often increase in frequency and severity with
time.
• Although SVT is usually not life-threatening, many patients
suffer recurrent symptoms that have a major impact on their
quality of life. The uncertain and sporadic nature of episodes of
tachycardia can cause considerable anxiety — many patients
curtail their lifestyle as a result, and many prefer curative
treatment.
• SVT often terminates before presentation, and episodes may
be erroneously attributed to anxiety.
• Sudden-onset, rapid, regular palpitations characterise SVT
and, in most patients, a diagnosis can be made with a high
degree of certainty from patient history alone. Repeated
attempts at electrocardiographic documentation of the
arrhythmia may be unnecessary.
• Treatment of SVT may not be necessary when the episodes are
infrequent and self-terminating, and produce minimal
symptoms.
• When episodes of tachycardia occur frequently, are prolonged
or are associated with symptoms that affect quality of life,
catheter ablation is the first choice of treatment; it is a low-risk
procedure with a high success rate. Long-term preventive
pharmacotherapy is an alternative approach in some patients.
MJA 2009; 190: 255–260
coronary disease or myocardial dysfunction. The symptoms of SVT
can be very similar to those of anxiety, and both may co-exist. Very
rapid heart rate (around 180–200 beats/min) and termination of
palpitations with the Valsalva manoeuvre are consistent with the
diagnosis of SVT.
Evaluating the patient with SVT
History
Classical SVT history is characterised by an abrupt onset of rapid
palpitations. This strongly suggests SVT, and diagnosis can usually
be made without electrocardiographic documentation. Gradual
onset of palpitations suggests sinus tachycardia,11 and irregular
palpitations often indicate atrial fibrillation.
Defining the frequency and duration of palpitations and associ-
ated symptoms enables an assessment of clinical severity. Episodes
of SVT may be triggered by factors including caffeine and alcohol
intake (which can increase the frequency with which ectopic beats
are triggered), bending over, sudden movements, stress, physical
exertion and fatigue. Patients will have a clear idea of whether any
of these are common triggers in their own case. When triggers are
present they should be avoided if possible, but there is no a priori
reason to restrict caffeine or alcohol intake or limit exercise in
patients for whom these are not triggers.
255

1 Types of supraventricular tachycardia and their
features
Atrioventricular nodal re-entrant tachycardia
• Most common form
• Re-entrant circuit involves the atrioventricular node
• Retrograde P waves may be seen buried within or just after the
QRS complex in tachycardia
Atrioventricular re-entrant tachycardia
• Second most common form
• Re-entrant circuit involves an accessory pathway
• Some pathways, termed “concealed” pathways, only conduct in a
retrograde direction
• Pathways that conduct in an antegrade direction show pre-
excitation on a surface electrocardiogram (Wolff–Parkinson–White
syndrome)
Atrial tachycardia
• Third most common form
• Tachycardia arises from a localised focus of atrial tissue
• Foci arise from characteristic locations in the atrium
• P-wave morphology can be used to identify the site of tachycardia
origin
Sinus tachycardias
Physiological sinus tachycardia
• Appropriate response to a physiological or pathological stress
Inappropriate sinus tachycardia
• Typically seen in women — usually in health care workers
• Persistent elevation of the sinus rate during the day, which
normalises during sleep
Postural orthostatic tachycardia syndrome
• Inappropriate sinus tachycardia associated with upright posture
• Other autonomic symptoms may coexist
Rare forms of supraventricular tachycardia
Permanent junctional reciprocating tachycardia
• Typically seen in children
• Associated with tachycardia-mediated cardiomyopathy
Junctional ectopic tachycardia
• Occurs in children
• Tachycardia arises from a discrete focus in the atrioventricular
node
Mahaim tachycardia
• Tachycardia due to an abnormal accessory pathway between the
atrioventricular node and His–Purkinje system
• Pathway usually inserts from the right atrium into the right ventricle
near the right bundle branch
Examination
Results of cardiovascular examination are usually normal for
patients with SVT, but signs of structural heart disease should be
sought.
Electrocardiogram
In many cases, results of a baseline electrocardiogram (ECG) in
patients with SVT are normal. However, the results should be
carefully evaluated for evidence of pre-excitation, defined by a
short PR interval (< 120 ms) and a delta wave (slurred upstroke at
the onset of the QRS complex) (Box 2). This is the classical ECG
appearance of Wolff–Parkinson–White (WPW) syndrome.12
256 MJA • Volume 190 Number 5 • 2 March 2009
R EV I E W
If the arrhythmia is captured on an ECG it is usually a narrow-
complex tachycardia (QRS duration, < 120 ms) (Box 3), but may
have a prolonged QRS interval (> 120 ms) when associated with
pre-existing or rate-related bundle branch block. In wide-complex
tachycardia, however, it is safest to assume that the tachycardia is
ventricular in origin until proven otherwise. A normal Holter
monitor reading is seen in most patients with SVT because of the
intermittent nature of episodes; thus a normal reading does not
exclude the diagnosis of SVT. Often, prolonged and multiple
unnecessary attempts at rhythm documentation are made when
the diagnosis is evident from clinical history. Occasionally, in
patients with infrequent palpitations and a less definite clinical
history, cardiac event recorders or implantable monitors may be
necessary to capture the underlying rhythm disturbance.
Echocardiogram
An echocardiogram can be used to evaluate cardiac structure and
function, but results are usually normal for patients with SVT.
Exercise testing
Exercise testing is less useful for diagnosis of SVT unless the
arrhythmia is typically triggered by exertion. Patients may com-
plain of chest discomfort or pain during SVT episodes. These
symptoms do not mandate an exercise stress test or angiography;
decisions on further testing should be based on history and
presence of vascular risk factors.
Mechanisms of SVT
Atrioventricular nodal re-entrant tachycardia
The most common type of SVT is AVNRT.13 The mechanism
involves a re-entrant circuit that includes the posterior inputs to
the compact atrioventricular node, anterior inputs to the node, and
probably perinodal atrial tissue. The tachycardia is often triggered
by an appropriately timed atrial ectopic beat (Box 4).
Atrioventricular re-entrant tachycardia
AVRT is the second most common type of SVT, and uses an
accessory pathway to complete the re-entrant circuit. Accessory
pathways are muscular connections composed of functional myo-
cardial fibres that directly connect the atria and ventricles, bypassing
the atrioventricular node. Many accessory pathways do not produce
pre-excitation on the ECG during sinus rhythm, owing to an
◆
inability to conduct in an antegrade direction. When the pathway
conducts from ventricle to atrium (retrograde conduction), with no
evidence of antegrade conduction on the sinus rhythm ECG, the
pathway is termed “concealed”. In this situation, the tachycardia
circuit involves antegrade conduction over the atrioventricular node
and retrograde conduction over the accessory pathway.
When the accessory pathway also conducts in the antegrade
direction during sinus rhythm, the ventricular myocardium is
activated earlier than if conduction occurred only through the
atrioventricular node, resulting in ventricular pre-excitation (WPW
syndrome, Box 2).12 In patients with WPW syndrome, episodes of
SVT can trigger atrial fibrillation leading to rapid conduction of the
atrial activity to the ventricle via the accessory pathway. Unlike the
atrioventricular node, which acts as a filter between the atria and
ventricles, an accessory pathway can transmit atrial rates of up to
 R EV I E W

Multifocal atrial tachycardia:

2 Electrocardiogram showing pre-excitation
This is characterised by elec-
trocardiographic evidence of at
least three different P-wave
morp holog ies. It usually
occurs in older patients with
chronic lung disease or con-
gestive cardiac failure, and
may ultimately disorganise
into atrial fibrillation.19

The PR interval is short (< 120 ms) and there is a slurred onset of the QRS complex, with a widened QRS
morphology. The appearance and degree of pre-excitation that is evident depends on the conduction of the
pathway and atrioventicular nodal conduction.
300 beats/min directly to the ventricles (Box 5). This can lead to
ventricular fibrillation and sudden death.14
Atrial tachycardia
Focal atrial tachycardia: This accounts for about 10% of cases of
SVT, and originates from a single localised focus of atrial tissue.15-17
The atrial rate can vary widely, from 120 beats/min to 300 beats/min.
Depending on the atrial rate, and on atrioventricular node conduc-
tion, the atria may conduct 1:1 to the ventricles, or with varying
degrees of atrioventricular block. Focal atrial tachycardia has
characteristic anatomical sites of origin. The most common site in
the right atrium is along the crista terminalis, and in the left atrium
common sites are the ostia of the pulmonary veins.16,18
Sinus tachycardias
Inappropriate sinus tachycardia:
This is an unusual clinical syn-
drome; it is characterised by a
persistently elevated resting
heart rate (> 100 beats/min) that
is disproportionate to the degree
of physiological and/or patho-
◆
logical stress. It is important to
eliminate secondary causes of
sinus tachycardia (eg, thyrotoxicosis, anaemia) before the diagnosis is
made. Enhanced automaticity of the sinus node, excess sympathetic
tone and reduced parasympathetic tone are the principal proposed
mechanisms.20 Most patients who are affected by inappropriate sinus
tachycardia are women, and it is particularly common in health care
workers — possibly because they are more likely to self-recognise
tachycardia than the general population.21 The condition is poorly
understood and, after secondary causes have been excluded, patients
may be misdiagnosed as having anxiety or a panic disorder. Monitor-
ing electrocardiographic function over a 24-hour period using a
Holter monitor is the most useful means of identifying inappropriate
sinus tachycardia; classically, it reveals a persistently elevated sinus
rate (> 100 beats/min) during the day and normalisation of the heart
rate during sleep.22

3 Twelve-lead electrocardiogram of a narrow-complex tachycardia

The lack of visible P waves suggests that this tachycardia is due to atrioventricular nodal re-entrant tachycardia, or atrioventricular re-entrant
tachycardia with a concealed pathway. ◆

MJA • Volume 190 Number 5 • 2 March 2009 257

 R EV I E W

Postural orthostatic tachycardia syn-

4 Holter monitor recording showing the initiation of supraventricular tachycardia
drome: In this syndrome an inappro-
triggered by an atrial ectopic beat
priate sinus tachycardia is associated
with upright posture, in the absence
of postural hypotension or auto-
nomic neuropathy.23 Symptoms over-
lap with those of inappropriate sinus
tachycardia, and additional auto-
nomic symptoms can occur —
tremor, constipation, bladder dysfunc-
tion, feeling cold, heat intolerance,
marked fatigue and exercise intoler-
ance.24 The symptoms and the accom-
panying sinus tachycardia can be
reproduced by tilt-table testing.22

Management of SVT

Short-term management
The goal of short-term management
is to terminate acute episodes of
tachycardia, which can often be
ach iev ed by man oeu vres that
increase vagal tone, including the
Valsalva manoeuvre, application of a
cold stimulus to the face and carotid
sinus massage. Carotid sinus massage
can also provide diagnostic informa-
tion by slowing atrioventricular nodal
conduction and exposing the P wave;
it is performed by applying gentle
pressure over one carotid sinus for 5–
10 seconds during held inspiration.
This manoeuvre should not be per-
formed if there is a history of carotid
artery disease or if carotid bruits are
detected on examination.
If vagal stimulation is unsuccess-
ful, recommended drugs include
adenosine, and calcium antagonists
such as verapamil or diltiazem.25
Adenosine is advantageous as its The P wave of the atrial ectopic beat is visible as a distortion of the T wave of the preceding beat
onset is instantaneous and it has an (solid arrow). Retrograde P waves are visible immediately after the QRS complex (dotted arrows).
extremely brief duration of action. This tachycardia may be due to atrioventricular re-entrant tachycardia with a concealed pathway, or
However, in rare cases it can aggra- atrioventricular node re-entry. This patient did not elect to undergo an electrophysiology study and
vate bronchospasm, cause atypical ablation therapy, and is not on maintenance medical therapy. ◆

chest discomfort or cause a sensation

of impending doom. Administered
by intravenous injection, a 6 mg dose of adenosine is successful in
reverting SVT in 75% of patients, and a 12 mg dose is successful in
more than 90% of patients.26 If adenosine therapy is unsuccessful,
intravenous boluses of either verapamil or diltiazem usually
27,28
terminate tachycardia, but carry the risk of potentiating hypo-
tension and bradycardia. Intravenous verapamil is more readily
available in most clinical settings than intravenous diltiazem. In
adults, 5–10 mg of verapamil administered by intravenous injec-
tion over 2–3 minutes is often successful in reverting SVT. Patients
given verapamil must be monitored due to the risk of bradycardia.
SVT resulting in haemodynamic instability is rare but necessitates
urgent direct-current cardioversion.
Long-term management
Long-term management is individualised based on the frequency
and severity of episodes and the impact of symptoms on quality of
life.29 For infrequent, self-terminating and minimally symptomatic
episodes, treatment is not necessarily required; however, many
patients will opt for a curative approach owing to the anxiety
associated with possible recurrence of symptomatic episodes.
Definitive treatment of SVT is indicated in patients who:
• have recurrent symptomatic episodes of SVT that affect their
quality of life;
• experience symptoms of SVT, and have WPW syndrome
detected on ECG; and

258 MJA • Volume 190 Number 5 • 2 March 2009

 R EV I E W

5 Twelve-lead electrocardiogram showing pre-excited atrial fibrillation

The accessory pathway is capable of very rapid conduction, resulting in a ventricular rate that is greater than if conduction occurred via the
atrioventicular node. At times, the ventricular rate approximates 300 beats/min (arrow). Catheter ablation is mandatory in this situation. ◆

• have infrequent episodes of SVT but are engaged in a profession
or sport in which an episode of SVT could put them or others at
risk (eg, pilots and divers).
Radiofrequency catheter ablation is recommended for most of
these patients. It has a low risk of complications, and is curative in
more than 95% of patients.30 The procedure typically takes 1–1.5
hours; it can be performed under local anaesthesia with sedation,
or under general anaesthesia. Patients usually stay in hospital
overnight after the procedure for cardiac monitoring and observa-
tion.
Pharmacological management
Long-term pharmacotherapy is generally used in patients who
decline catheter ablation, and in whom the procedure carries an
unacceptably high risk of atrioventricular node injury and pace-
maker dependence. The goal of long-term pharmacotherapy is to
reduce the frequency of episodes of SVT. In only a small minority
of patients will episodes be completely abolished by antiarrhyth-
mic drugs. Recommended drugs include atrioventricular nodal
blocking drugs and antiarrhythmic drugs of Class Ic and Class III.
Beta blockers and calcium-channel blockers (Class II and IV) are
suitable first-line treatments when WPW syndrome is not detected
on a surface ECG. Randomised studies have not demonstrated
clinical superiority of any single agent, but beta blockers and
calcium-channel blockers are perceived to be superior to digoxin
as they provide better atrioventricular nodal blocking action
during states of high sympathetic tone, such as exercise.31 Digoxin
should not be used in patients with WPW syndrome, as it may
facilitate rapid conduction over the accessory pathway during
atrial fibrillation — potentially leading to ventricular fibrillation.32
Combining atrioventricular nodal blocking agents increases effi-
cacy, but also increases adverse effects.33
For patients who do not respond to these drugs, or for those
with WPW syndrome, alternative drugs include flecainide (Class
Ic actions) and sotalol (Class II and Class III actions). Flecainide
and sotalol are more effective than atrioventricular nodal blockers
in terms of preventing SVT, but are associated with a small a risk of
ventricular tachycardia. This risk is small in patients without
structural heart disease, but it is has been reported to occur in 1%–
3% of patients taking sotalol, particularly those taking higher
doses.34,35 Amiodarone has no role in long-term prevention of
SVT, owing to the high incidence of serious toxicities associated
with its long-term use.36
Beta blockers are first-line therapy for the management of inap-
propriate sinus tachycardia; the dose should be titrated to balance
symptom control with prevention of hypotension and bradycar-
dia.22 Verapamil and diltiazem are alternatives for patients in whom
beta blockers are contraindicated. A new agent, ivabradine, acts by
blocking the sodium current responsible for spontaneous depolari-
sation in the sinus node (If), which results in sinus bradycardia.37
Ivabradine has no negative inotropic effects but may produce visual
disturbance that is reversible on discontinuation of the drug. It is
licensed for treating angina and, although there is relatively little
published data on its efficacy, it may be trialled off-label in patients
with inappropriate sinus tachycardia who do not respond to beta
blockers and calcium-channel blockers. In patients with postural
orthostatic tachycardia syndrome, increased fluid and salt intake,
resistance exercises, squatting and compressive stockings may be
effective.38 When non-pharmacological strategies are ineffective,
beta blockers and/or fludrocortisone may be beneficial.22

MJA • Volume 190 Number 5 • 2 March 2009 259

 R EV I E W
Competing interests
None identified.
Author details
Caroline Medi, BMed, FRACP, Electrophysiology and Pacing Fellow1,2
Jonathan M Kalman, MB BS, PhD, FRACP, Director of
Electrophysiology,1 and Professor of Medicine2
Saul B Freedman, MB BS, PhD, FRACP, Professor of Cardiology3,4
1 Department of Cardiology, Royal Melbourne Hospital, Melbourne,
VIC.
2 Department of Medicine, University of Melbourne, Melbourne, VIC.
3 Department of Cardiology, Concord Clinical School, Concord
Hospital, Sydney, NSW.
4 Vascular Biology Laboratory, ANZAC Research Institute, University of
Sydney, Sydney, NSW.
Correspondence: jon.kalman@mh.org.au
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(Received 15 Jun 2008, accepted 2 Oct 2008) ❏